1. Dr Ibraheem bashayreh, RN, PhD
Cirrhosis of the Liver
Dr Ibraheem bashayreh, RN, PhD

2. ANATOMY & PHYSIOLOGY LIVER
Weighing between 1,200 and 1,600 g, the liver is the largest glandular organ in the body. It is located in the right upper abdominal quadrant, under the right diaphragm.
The liver is divided into four lobes: left, right, caudate and quadrate. The lobes are further subdivided into smaller units known as lobules.
The liver contains several cell types including hepatocytes (ie. Liver cells) and Kupffer cells (i.e. phagocytic cells that engulf bacteria).
Bile is continuously formed by hepatocytes (about 1L/day). Bile comprises water, electrolytes , lecithin,fatty acids, cholesterol, bilirubin and bile salts.
The Liver is surrounded by a tough fibroelastic capsule called Glisson’s capsule. 2

4. FUNCTIONS OF THE LIVER
Regulating blood glucose level by making glycogen, which is stored in hepatocytes.
Synthesizing blood glucose from amino acids of lactate through gluconeogenesis.
Converting ammonia produced from gluconeogenetic by-products and bacteria to urea
Synthesizing plasma proteins such as albumin, globulins, clotting factors, and lipoproteins.
Breaking down fatty acids into ketone bodies
Storing vitamins and trace metals
Affecting drug metabolism and detoxification
Secreting bile 4

6. Liver cirrhosis

7. Description Extensive parenchymal cell degeneration
A chronic, progressive disease of the liver
Extensive parenchymal cell degeneration
Destruction of parenchymal cells

8. Description
Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis

9. Description
Normal lobular structure distorted by fibrotic connective tissue
Lobules are irregular in size and shape with impaired vascular flow
Insidious, prolonged course

10. Etiology and Pathophysiology
Cell necrosis occurs
Destroyed liver cells are replaced by scar tissue
Normal architecture becomes nodular

11. Etiology and Pathophysiology
Four types of cirrhosis:
Alcoholic (Laennec’s) cirrhosis
Postnecrotic cirrhosis
Biliary cirrhosis
Cardiac cirrhosis

12. Etiology and Pathophysiology
Alcoholic (Laennec’s) Cirrhosis
Associated with alcohol abuse
Preceded by a theoretically reversible fatty infiltration of the liver cells
Widespread scar formation

13. Etiology and Pathophysiology
Postnecrotic Cirrhosis
Complication of toxic or viral hepatitis
Accounts for 20% of the cases of cirrhosis
Broad bands of scar tissue form within the liver

14. Etiology and Pathophysiology
Biliary Cirrhosis
Associated with chronic biliary obstruction and infection
Accounts for 15% of all cases of cirrhosis

15. Etiology and Pathophysiology
Cardiac Cirrhosis
Results from longstanding severe right-sided heart failure

16. Manifestations of Liver Cirrhosis
Fig. 42-5

17. Clinical Manifestations Early Manifestations
Onset usually insidious
GI disturbances:
Anorexia
Dyspepsia
Flatulence
N-V, change in bowel habits

18. Clinical Manifestations Early Manifestations
Abdominal pain
Fever
Lassitude (laziness)
Weight loss
Enlarged liver or spleen

19. Clinical Manifestations Late Manifestations
Two causative mechanisms
Hepatocellular failure
Portal hypertension

20. Clinical Manifestations Jaundice
Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

21. Clinical Manifestations Jaundice
Intermittent jaundice is characteristic of biliary cirrhosis
Late stages of cirrhosis the patient will usually be jaundiced

23. Clinical Manifestations Skin
Spider angiomas (telangiectasia, spider nevi)
Palmar erythema

24. Clinical Manifestations Endocrine Disturbances
Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

25. Clinical Manifestations Endocrine Disturbances
Alteration in hair distribution
Decreased amount of pubic hair
Axillary and pectoral alopecia

26. Clinical Manifestations Hematologic Disorders
Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

27. Clinical Manifestations Hematologic Disorders
Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

28. Clinical Manifestations Peripheral Neuropathy
Dietary deficiencies of thiamine, folic acid, and vitamin B12

29. Complications Portal hypertension and esophageal varices
Peripheral edema and ascites
Hepatic encephalopathy
Fetor hepaticus: is bad breath with a 'dead mouse' or sweet faecal smell. ... It may be caused by severe hepatocellular damage

30. Complications Portal Hypertension
Characterized by:
Increased venous pressure in portal circulation
Splenomegaly
Esophageal varices
Systemic hypertension

31. Complications Portal Hypertension
Primary mechanism is the increased resistance to blood flow through the liver

32. Complications Portal Hypertension Splenomegaly
Back pressure caused by portal hypertension  chronic passive congestion as a result of increased pressure in the splenic vein

33. Complications Portal Hypertension Esophageal Varices
Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

34. Complications Portal Hypertension Esophageal Varices
Varices have fragile vessel walls which bleed easily

35. Complications Portal Hypertension Internal Hemorrhoids
Occurs because of the dilation of the mesenteric veins and rectal veins

36. Complications Portal Hypertension Caput Medusae
Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

37. Complications Peripheral Edema and Ascites
- Intraperitoneal accumulation of watery fluid containing small amounts of protein

38. Complications Peripheral Edema and Ascites
Factors involved in the pathogenesis of ascites:
Hypoalbuminemia
 Levels of aldosterone
 Portal hypertension

40. Complications Hepatic Encephalopathy
Liver damage causes blood to enter systemic circulation without liver detoxification

41. Complications Hepatic Encephalopathy
Main pathogenic toxin is NH3 although other etiological factors have been identified
Frequently a terminal complication

42. Complications Fetor Hepaticus
Musty, sweetish odor detected on the patient’s breath
From accumulation of digested by-products

43. Development of Ascites
Fig. 42-6

44. Diagnostic Studies Liver function tests Liver biopsy Liver scan
Liver ultrasound

45. Diagnostic Studies Esophagogastroduodenoscopy Prothrombin time
Testing of stool for occult blood

46. Collaborative Care Rest Avoidance of alcohol and anticoagulants
Management of ascites

47. Collaborative Care
Prevention and management of esophageal variceal bleeding
Management of encephalopathy

48. Collaborative Care Ascites
High carbohydrate, low protein, low Na+ diet
Diuretics
Paracentesis

49. Collaborative Care Ascites
Peritoneovenous shunt
Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

50. Peritoneovenous Shunt
Fig. 42-8

51. Collaborative Care Esophageal Varices
Avoid alcohol, aspirin, and irritating foods
If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)

52. Collaborative Care Esophageal Varices
Endoscopic sclerotherapy or ligation
Balloon tamponade
Surgical shunting procedures (e.g., portacaval shunt, TIPS)

54. Sengstaken-Blakemore Tube
Fig. 42-9

55. Portosystemic Shunts
Fig

56. Collaborative Care Hepatic Encephalopathy
Goal: reduce NH3 formation
Protein restriction (0-40g/day)
Sterilization of GI tract with antibiotics (e.g., neomycin)
lactulose (Cephulac) – traps NH3 in gut
levodopa

57. Drug Therapy There is no specific drug therapy for cirrhosis
Drugs are used to treat symptoms and complications of advanced liver disease

58. Nutritional Therapy Diet for patient without complications:
High in calories
 CHO
Moderate to low fat
Amount of protein varies with degree of liver damage

59. Nutritional Therapy Patient with hepatic encephalopathy
Very low to no-protein diet
Low sodium diet for patient with ascites and edema

60. Nursing Management Nursing Assessment
Past health history
Medications
Chronic alcoholism
Weight loss

61. Nursing Management Nursing Diagnoses
Imbalanced nutrition: less than body requirements
Impaired skin integrity
Ineffective breathing pattern
Risk for injury

62. Nursing Management Planning
Overall goals:
Relief of discomfort
Minimal to no complications
Return to as normal a lifestyle as possible

63. Nursing Management Nursing Implementation
Health Promotion
Treat alcoholism
Identify hepatitis early and treat
Identify biliary disease early and treat

64. Nursing Management Nursing Implementation
Acute Intervention
Rest
Edema and ascites
Paracentesis
Skin care
Dyspnea
Nutrition

65. Nursing Management Nursing Implementation
Acute Intervention
Bleeding problems
Balloon tamponade
Altered body image
Hepatic encephalopathy

66. Nursing Management Nursing Implementation
Ambulatory and Home Care
Symptoms of complications
When to seek medical attention
Remission maintenance
Abstinence from alcohol

67. Nursing Management Evaluation
Maintenance of normal body weight
Maintenance of skin integrity
Effective breathing pattern
No injury
No signs of infection

68. Gallbladder Disorders

69. ANATOMY & PHYSIOLOGY BILIARY SYSTEM
Canaliculi – the smallest bile ducts located between liver lobules, receive bile from hepatocytes. The canaliculi form larger bile ducts, which lead to hepatic duct.
Hepatic duct – from the liver joins the cystic duct from the gallbladder to form the common bile duct, which empties into the duodenum.
Sphincter of Oddi – controls the flow of bile into the intestine.
Gallbladder – is a hollow pear-shaped organ that is 30-40mm long. Normally holds 30-50mL of bile and can hold up to 70mL when fully distended.

70. BILIARY SYSTEM
Draining bile from hepatocytes to the gallbladder by way of biliary tree
Storing bile in the gallbladder and releasing it to the duodenum, which is mediated by the hormone cholecystokinin-pancreozymin.

71. The Gallbladder
Located below the liver
The cystic duct joins the hepatic duct to become the bile duct
The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum

72. Stores and concentrates bile
Contracts during the digestion of fats to deliver the bile
Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi 72

74. CHOLELITHIASIS
Refers to formation of calculi (ie, gallstones in the bladder.
Predisposing Factors:
Obese
Female
>40 yrs
OC, Estrogen, intake
Fair 74

75. CHOLELITHIASIS Supersaturated bile, Biliary stasis Stone formation
Blockage of Gallbladder
Inflammation, Mucosal Damage and WBC infiltration
CHOLECYSTITIS 75

76. Common locations of gallstones

78. Gall Stones

79. CHOLECYSTITIS – inflammation of gallbladder with gallstone formation.
GALLBLADDER – storage of bile – made up of cholesterol. 79

80. PATHOLOGY-SIGNS AND SYMPTOMS

81. CHOLECYSTITIS/ CHOLELITHIASIS
Signs and Symptoms:
Severe Right abdominal pain radiating to the back
Fever
Fat intolerance
Anorexia, n/v
Jaundice
Pruritus
Easy bruising
Tea colored urine
Steatorrhea 81

82. CHOLECYSTITIS/ CHOLELITHIASIS
Diagnosis:
US detects the presence of gallstone
Serum alkaline phosphatase – u/L
WBC
Endoscopic retrograde cholangiopancreatography (ERCP) - 82

83. CHOLECYSTITIS/ CHOLELITHIASIS
Nursing Management:
Administer Rx Medications
Diet – increase CHO, moderate CHON, decrease fats
Meticulous skin care
Instruct patient to AVOID HIGH- fat diet and GAS-forming foods
Assist in surgical and non-surgical measures
ESWL – non-invasive fragmentation of stones by using repeated shockwaves directed at the gallstones in the gallbladder or common bile duct. 83

84. CHOLELITHIASIS/CHOLECYSTITIS
Surgical procedures- Surgical Cholecystectomy, Choledochotomy,
Laparoscopic cholecystectomy 84

87. CHOLELITHIASIS/CHOLECYSTITIS
Post-operative nursing interventions
1. Monitor for surgical complications
2. Post-operative position after recovery from anesthesia- LOW FOWLER’s
3. Encourage early ambulation
4. Administer medication before coughing and deep breathing exercises
5. Advise client to splint the abdomen to prevent discomfort during coughing
6. Administer analgesics, antiemetics, antacids
7. Care of the biliary drainageor T-tube drainage
8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed 87